Immune signaling networks determine how host cells integrate environmental cues, coordinate multiple inputs, and sustain or resolve inflammation. These processes are governed not by individual receptors, but by system-level signaling programs whose strength, timing, and persistence shape immune behavior. Dysregulation of these programs underlies a broad spectrum of chronic inflammatory conditions, ranging from localized inflammatory states to systemic autoimmune diseases, neurodegenerative disorders, and cancer; however, the principles by which immune signaling becomes maladaptive and self-sustaining remain poorly defined.

Our laboratory investigates the fundamental mechanisms of immune signal integration using a systems-based framework, with a focus on how microbiome-derived and endogenous cues reprogram innate immune signaling to drive persistent inflammatory states. Rather than studying isolated pathways, we examine how immune cells integrate cytosolic and surface-derived signals over time, how feedback and feedforward loops stabilize signaling programs, and how these dynamics generate durable immune phenotypes associated with chronic disease pathogenesis.

A defining aspect of our work is the development of quantitative, pathway-resolved analytical frameworks to measure immune signaling potency, kinetics, and persistence. These approaches enable standardized comparisons across microbial stimuli, cellular states, and human clinical samples, supporting reproducibility, scalability, and translational interpretation. This quantitative framework facilitates the identification of immune signatures that link exposures to microbial, environmental, and localized inflammation to disease trajectories in autoimmunity, neuroinflammation, and cancer.

Our research emphasizes the temporal and spatial organization of immune signaling, examining how late-phase responses diverge from early activation events and how intracellular signal compartmentalization contributes to sustained immune states. We also investigate how cellular differentiation and immune context determine signaling capacity, providing insight into inter-individual variability and disease heterogeneity.

By integrating immunology and microbiology with biochemistry, molecular biology, systems biology, multi-omics analytics, advanced imaging, and computational modeling, our laboratory captures immune signaling as a coordinated biological system. Human clinical samples are central to this work, ensuring biological relevance and translational applicability.

Ultimately, our goal is to define generalizable, quantitative principles governing immune signal persistence and to translate these insights into predictive biomarkers and targeted therapeutic strategies for localized chronic inflammatory diseases and associated comorbidities, including autoimmune disorders, neurodegenerative diseases, and cancer.